Barron's Medical Journal

Friday, November 29, 2013

The FDA Set Back Science One Hundred Years Barron’s Medical Suggest Start With Breast Cancer 23 And Me

Barron’s Medical Journal Reporting From Harvard University Boston, MA USA

The FDA Set Back Science One Hundred Years Barron’s Medical Suggest Start With Breast Cancer 23 And Me

Boston MA ( AP )The most dangerous thing the Federal Drug Administration has done in the last one hundred and fifty Years. Was to step in to the greatest thing to happen to science in one hundred years. Says Rose Conrad The CEO of Sam Houston Medical Software a Houston, Texas Base Company that specialized in Genomics Science. Conrad says the entire science community in the United States was elated when Google the Internet Search Company invested in a company called 23 and Me. For Ninety Nine dollars you can get a entire Genetic test for ninety nine dollars. Out of the blue was sent a letter by the FDA to stop selling the test. Anne Wojcicki, co-founder of $99 DNA testing service 23andMe, countered a warning letter issued by the Food and Drug Administration demanding the company "immediately discontinue marketing" its DNA testing kit. "We stand behind the data that we return to customers—but we recognize that the FDA needs to be convinced of the quality of our data as well," Wojcicki said in a blog post on the company's website Tuesday night.a On Nov. 22 the FDA ordered 23andMe to halt marketing of its genetic testing device, expressing concern that it could return inaccurate results and lead consumers to undergo unnecessary health procedures.

Did you know that we have a breast cancer treatment model that has not changed in many Physicians offices since 1970? In 1970 A MCF-7 is a breast cancer cell line isolated in 1970 from a 69-year-old Caucasian woman. MCF-7 is the acronym of Michigan Cancer Foundation - 7, referring to the institute in Detroit where the cell line was established in 1973 by Herbert Soule and co-workers The Michigan Cancer Foundation is now known as the Barbara Ann Karmanos Cancer Institute.

This is why we now have analytics that says that fifty percent of the Women in the United States that get chemotherapy do not need it. This is why that so many reports says that Black women get breast cancer and a rate of 18% and White women a rate of 7% . Prior to MCF-7, it was not possible for cancer researchers to obtain a mammary cell line that was capable of living

longer than a few months, since the 1950’s when this car was created a big change in the way we treat breast cancer patients in 1970… Now In 2012 we are making another major change. The Change is a Medical Technology Called Genomics. The patient, whose name, Frances Mallon, is unknown to the vast majority of cancer researchers, died in 1970. Her cells were the source of much of current knowledge about breast cancer Scientist around world is working with genomics. For an example, The International Cancer Genome Consortium (ICGC) today announced four new projects in China to identify the genomic drivers in colorectal, esophageal, liver and nasopharyngeal cancers, helping lay the foundation for developing treatments tailored to patients’ individual needs. China is a founding member of the ICGC, having launched a gastric cancer project in 2008.

The Consortium leads worldwide efforts to map the genomes of both common and rare cancers and has the goal of identifying cancer-causing mutations in more than 25,000 tumors representing more than 50 types of cancer of clinical and societal importance across the globe. Houston base companies like Sam Houston Biotech found involvement in human breast cancer progression, based on the analysis of human breast cancer biopsies and experimental animal mice models. HIF-1 as a therapeutic target can extend the life of many stage four breast Cancer patients. 

Sam Houston discovered The tumor suppressors VHL (von Hippel-Lindau protein) and p53 target HIF-1α for ubiquitination to inactivation breast cancer tumors cells increases the of HIF-1. This process Increased phosphatidylinositol 3-kinase (PI3K) and AKT. In breast cancer, increased activity of the HER2 (also known as neu) receptor tyrosine kinase is associated with increased tumor grade, chemotherapy resistance, and decreased patient survival. HER2 has also been implicated as an inducer of VEGF expression. Sam Houston demonstrate that HER2 signaling induced by overexpression in mouse 3T3 cells or human MCF-7 breast cancer cells results in increased HIF-1α protein and VEGF mRNA expression that is dependent upon activity of PI3K, AKT (also known as protein kinase B), and the downstream kinase FRAP (FKBP-rapamycin-associated protein) Sam Houston concern with patients with diabetes and breast cancer may not receive full Benefit of HIF-1. All women having access to a physician can have access to HIF-1. Genomics provide a faster cheaper more effective way to detecting Breast Cancer by using Semiconductor Sequencing.

A example of this technique is Sam Houston Semiconductor Sequencing. "Quantum Theory" In Action for Breast Cancer Patients. A polymerase is an enzyme whose central function is associated with polymers of nucleic acids such as RNA and DNA. The primary function of a polymerase is the polymerization of new DNA or RNA against an existing DNA or RNA template in the processes of replication and transcription. In association with a Sam Houston also uses a Visualize Real-Time Breast Cancer Data using Signal Stochastic Resonance Units Neurons Detection and Analysis for Breast Cancer model after McCulloch-Pitts. Gennxeix. computer-assisted diagnosing of breast cancer from mammograms. Sam Houston works is a genetic network simulation trained with tumor incidence data from knockout experiments.  Sam Houston uses Semiconductor Sequencing Chips that create a direct connection between Biochemical and digital information, bringing these two languages together. Gennxeix's chips are designed like any other semiconductor chips.  Pairing proprietary semiconductor technology with sequencing chemistry a nucleotide is incorporated into a strand of DNA by a polymerase, a hydrogen ion is released. Sam Houston used a high-density array of micro-machined wells for bioctechnology process in a massive way. Each well holds a different DNA template. Beneath the wells is an ion-sensitive layer and beneath that a proprietary Ion sensor.  Genomics can be the GPS to Extend life in Breast Cancer Patients. Barron's Medical Journal reported that hope for young women, those under 35, who get breast cancer out of the blue – especially because they are far more likely than older women to have a hard-to-treat type of breast cancer called triple negative breast cancer. A chemotherapy treatment called neoadjuvant chemotherapy can actual reduce the size of large triple negative breast cancer tumors. The efficacy of neoadjuvant chemotherapy, as measured by the rate of pathological complete response (the absence of invasive and intraductal disease in the breast and the axillary lymph nodes), varies according to breast-cancer subtype. When anthracyclines, taxanes, and agents directed against anti–human. First degree relatives of Breast Cancer Patients that take a Genomic test and find that the genes P53, P63, Her-2 and more are the largest candidates neoadjuvant chemotherapy treatments. A Houston base company called Sam Houston researcher work product. lets discuss some of their finding. Sam Houston discovered that some patients with HER2-positive breast cancer tended not respond to HER2-targeted therapies. Also, some patients with triple-negative breast cancers responded to therapies while others didn't. "We have been lumping things together that shouldn't be lumped together The new classifications - four types called HER2 "enriched," luminal A, luminal B and basal-like - categorize breast cancers by their genomic structure using a dizzying array of data points not previously available that have identified new pathways for the cancer to do its damage, making it possible for researchers to identify new places to target disease.

Anne Wojcicki, named "Most Daring CEO" by "Fast Company" magazine. Her start-up, 23andMe, lets consumers learn about their medical future with a $99 DNA test.

Wojcicki said her company has worked extensively with lab partners to ensure that all testing results are accurate, but she acknowledged that the company was "behind schedule" in responding to the FDA's request for more information, which resulted in the product's lack of marketing clearance. "This is new territory for both for 23andMe and the FDA," Wojcicki said. "This makes the regulatory process with the FDA important because the work we are doing with the agency will help lay the groundwork for what other companies in this new industry do in the future." Wojcicki, who recently separated from Google co-founder Sergey Brin, co-founded 23andMe in 2006. Google is an investor in the company. The FDA gave the company 15 working days to respond to its letter and outline the steps it is taking to address the agency's concerns. Recently, the Food and Drug Administration sent a letter to 23andMe telling the company to stop marketing its DNA testing kits, because the kits require FDA approval, which the company had not obtained. The letter emphasizes the need for 23andMe to prove that their tests are accurate. "FDA is concerned about the public health consequences of inaccurate results from the [Personal Genome Service] device; the main purpose of compliance with FDA's regulatory requirements is to ensure that the tests work," the letter reads, referring to 23andMe's genetic testing product.

However, according to one expert, the accuracy of the test is not the biggest issue. The company's testing methods have been found to meet federal standards for lab testing, called Clinical Laboratory Improvement Amendments (CLIA), said Amy Sturm, a genetic counselor at The Ohio State University Wexner Medical Center.

A greater problem is that the results provide "a very incomplete view" of a person's risk for a given disease, Sturm said. Limited view.

The company says that its DNA testing kit and analysis — which have been sold in the United States for more than five years, according to the FDA — can tell people whether their genes indicate an increased risk for more than 250 diseases and conditions. To do so, the test identifies certain genetic markers, or single nucleotide polymorphisms (SNPs), which are single spots in the DNA that vary among people and have been linked in research studies to diseases. But for many of these diseases, the company tests just a few genetic markers, when in reality, many other factors, including additional genetic markers, likely contribute to the development of the diseases, Sturm said. For example, to assess breast cancer risk, the test relies on three SNPs within the breast cancer genes BRCA1 and BRCA2, and eight other markers (SNPs) linked with breast cancer.

"The fact of the matter is … that's just such a limited view of breast cancer genetics," Sturm said. Researchers suspect that hundreds, if not thousands, of genetic markers likely influence breast cancer risk. And so even if people do not have those three SNPs, they could still have a genetic mutation that puts them at risk for breast cancer. The company also does not obtain a family history, or take into account environmentalfactors that may contribute to disease risk. [6 Foods That May Affect Breast Cancer Risk.

For instance, 23andMe provides a report on a person's risk of type 2 diabetes, but genetics contributes to just 26 percent of a person's risk, according to the company. The rest is due to environmental factors, such as obesity, physical inactivity and a history of heart disease, 23andMe said. And there are still unknown genetic factors that the test cannot take into account "It's just a very small snapshot of anyone's particular risk," said Barbara Bernhardt, a genetic counselor and professor of medicine at the University of Pennsylvania School of Medicine.

While 23andMe does explain that its tests do not take into account all of the factors that contribute to disease risk, that won't necessarily stop people from getting the wrong idea, Sturm said.

For example, a few years ago, Sturm counseled a man who had questions about his 23andMe results. The man was very concerned about his risk of esophageal cancer, based on his results. But after taking the man's family history, Sturm found out the man should be more worried about heart disease, which ran in his family, than esophageal cancer, Sturm said. And the increased risk of esophageal cancer discussed in the 23andMe report was based on a single genetic marker that had been studied only in a Chinese population, Sturm said. (The man was not Chinese, so it was unclear if the results applied to him, Sturm said.)

This counseling experience highlights another major issue with direct-to-consumer genetic tests: Consumers can take them without going through their health-care providers, experts say. "The danger is just, most people do not have the educational background to fully understand [the tests] themselves, what the result means," Sturm said.

Bernhardt agreed. "Since the beginning, the main concern has been about the potential for misunderstanding of the results, and the lack of resources that may be available to people to help sort out results," she said.

If people's results show they are at average risk for a disease, they might be overly reassured by the finding; and if the results show they are at increased risk, they may seek medical tests that they do not need, Sturm said. For instance, the man Sturm counseled kept asking if he needed a screening test for esophageal cancer, when he did not need one.

However, 23andMe does advise consumers to speak with their doctors if they have concerns about their results, and also offers to connect people with genetic counselors to explain results. But it's unclear how many people take advantage of these services, Sturm said.

In addition, people who take a genetic test through their doctors would likely undergo pre-test counseling to discuss what the results might reveal, and whether the patient would be ready to deal with such results. People who take the 23andMe test don't need to undergo pre-test counseling, even though the results might show a genetic risk for conditions such as Alzheimer's disease.

We have to move the Ball forward FDA stop this Maddnes.

Thursday, November 14, 2013

Is Amy Robach Making The Right Breast Cancer Treatment Choice At 40

Barron's Medical Journal Reporting From Duke University Medical School Durham, NC USA (Global Newswire )(AP News)

Is Amy Robach Making The Right Breast Cancer Treatment Choice At 40

Durham, NC (AP) After Good Morning America’s Amy Robach was diagnosed with Breast Cancer Barron’s Medical Journal Asked The CEO Of Sam Houston Biotech Inc Rose Conrad what she taught of the announcement ? Rose was happy to see that so many Women will now take notice and be willing to take a test at forty years of age to see if they are candidates for breast cancer. Conrad went on to say, why did Good Morning America not include A Genomic Test as part of the breast cancer testing process.

Genomics is a discipline in genetics that applies recombinant DNA, DNA sequencing methods, and bioinformatics to sequence, assemble, and analyze the function and structure of genomes (the complete set of DNA within a single cell of an organism). We then ask Rose is her company Doing any work with Genomics for breast cancer and if so explain the process. Genomics is the Gaussian processes in action, to predict the likelihood of chemotherapy benefit as well as recurrence, for patients with node-negative breast cancer that is estrogen-receptor positive and/or progesterone-receptor positive. Additionally, physicians use Sam Houston to make treatment recommendations for certain node-positive breast cancer patients, and the test report also provides quantitative scores for select individual genes. Sam Houston has been extensively evaluated in thirteen clinical studies involving more than 4,000 breast cancer patients worldwide, including a large validation study published in The New England Journal of Medicine and a chemotherapy benefit study published in the Journal of Clinical Oncology. Both Medicare and private health plans covering over 90 percent of U.S. insured lives provided reimbursement for Sam Houston for patients with node-negative breast cancer that is estrogen-receptor positive and/or progesterone-receptor positive through contracts, agreements or policy decisions.

Breast Cancer Researchers and Scientist are ahead of the curve with several new technologies based on Nanoparticles and Semi Conductors Namely Genomics and treatments. The field of genomics is caught in a data deluge. Targeted breast cancer DNA sequencing is becoming faster and cheaper at a pace far outstripping Moore’s law, which describes the rate at which computing gets faster and cheaper.

The result is that the ability to determine Targeted breast cancer DNA sequences is starting to outrun the ability of researchers to store, transmit and especially to analyze the data.

The cost of sequencing a human genome — all three billion bases of DNA in a set of human chromosomes — plunged to $10,000.00 which means genomics breast cancer DNA sequencing is around $3000.00.

The lower cost, along with increasing speed, has led to a huge increase in how much breast Cancer sequencing data is being produced.

Numerous investigations have shown that both tissue and cell distribution profiles of anticancer drugs can be controlled by their entrapment in submicronic colloidal systems (nanoparticles). The rationale behind this approach is to increase antitumor efficacy, while reducing systemic side-effects. This review provides an update of tumor targeting with conventional or long-circulating nanoparticles. The in vivo fate of these systems, after intravascular or tumoral administration, is discussed, as well as the mechanism involved in tumor regression. Nanoparticles are also of benefit for the selective delivery of oligonucleotides to tumor cells. Moreover, certain types of nanoparticles showed some interesting capacity to reverse MDR resistance, which is a major problem in chemotherapy. The first experiments, aiming to decorate nanoparticles with molecular ligand for active targeting of cancerous cells

Miniaturization will allow the tools for many different tests to be situated together on the same small device. Hybrid Sam Houston Researchers Say that nanotechnology will allow them to run many diagnostic tests simultaneously.

Nanoparticles nanoshells is use to antibodies that recognize cancer cells. Sam Houston scientist envision letting these nanoshells seek out their cancerous targets, then applying near-infrared light. The heat generated by the light-absorbing nanoshells can successfully killed breast cancer tumor cells while leaving neighboring cells intact.

A nanometer is a billionth of a meter. It's difficult to imagine anything so small, but think of something only 1/80,000 the width of a human hair. Ten hydrogen atoms could be laid side-by-side in a single nanometer.

Sam Houston minuscule molecule that will be used to detect breast cancer is a quantum dot. Quantum dots are tiny crystals that glow when they are stimulated by ultraviolet light. The wavelength, or color, of the light depends on the size of the crystal. Latex beads filled with these crystals can be designed to bind to specific DNA sequences. Hybrid Sam Houston understands that Hyperthermia gold nanoshell Targeted breast cancer genomics at 40 for high risk women will reduce breast cancer at 60 years of Age. Training Genomics Counselor and Storing DNA Analysis in the cloud will allow Hybrid Sam Houston to say that Chemotherapy will help their breast cancer outcome or if Chemotheraphy and Hyperthermia will extend their life.

The impact of genomics and pharmacogenomics in the current arena of clinical oncology is well-established. In breast cancer, mutations in the BRCA1 and BRCA2 genes have been well-characterized to carry a high risk of the disease during a woman's lifespan. However, these high risk genes contribute to only a small proportion of the familial cases of breast cancer. Hence, further efforts aimed to study the contribution of genetic mutations in other genes, including the estrogen receptor gene, TP53, CYP19, and mismatch repair genes to further investigate the genetic component of breast cancer.

Multiple pharmacogenomic studies have previously linked genetic variants in known pathways with treatment response in cancer patients. Currently, polymorphisms in drug metabolizing enzymes, efflux transporters, as well as, drug targets have shown correlations to variations in response and toxicity to commonly prescribed chemotherapeutic treatments of breast cancer. CYP2D6 variants have been correlated with tamoxifen response and interindividual variability seen. An emerging application of cancer genetics and pharmacogenetics involves the use of inherited or acquired genetic abnormalities to predict treatment toxicity or outcomes. Recently, methods that involve the scanning of entire genomes for common variants have begun to influence studies of cancer causation. Currently, treatment individualization for breast cancer can take place on the basis of few molecular targets including the estrogen receptor and the overexpression of the HER2 receptor. Overall, the current review summarizes the recent findings in the genetic and pharmacogenetic research of breast cancer and the advances made in personalization of treatment.

Women that use a Genomic Breast Cancer Test at 40 has a eighty seven percent chance to make sixty

Tuesday, November 5, 2013

Want To Know The Power Of Breast Cancer Research Funding Perjeta

Want To Know The Power Of Breast Cancer Research Funding Perjeta

Barron’s Medical Journal Reporting from The University Of Texas Medical School Houston, Texas USA

Houston ( AP ) Barron’s Medical Journal is at The University of Texas Medical School to bring you the latest in breast cancer research. Yes there is a new kid on the block for breast cancer Perjeta. Perjeta was only used for Women that had stage four breast cancer and now thanks to millions of dollars spent on breast cancer research the FDA has approved Perjeta to be use in Stage one breast cancer. This is fantastic news and the power of genomics science what use to take years now companies like Roche and other are using genomic to speed up their research.

United States (U.S.) Food and Drug Administration (FDA) granted accelerated approval of a Perjeta (pertuzumab) regimen for neoadjuvant treatment (use before surgery) in people with high-risk, HER2-positive early stage breast cancer. This approval is based primarily on data from a Phase II study showing that nearly 40 percent of people receiving the combination of Perjeta, Herceptin (trastuzumab) and docetaxel chemotherapy had no evidence of tumour tissue detectable at the time of surgery (known as a pathological complete response, or pCR). The Perjeta regimen is the first neoadjuvant breast cancer treatment approved by the FDA and also the first to be approved based on pCR data.

The approval of pertuzumab for neoadjuvant treatment of breast cancer is based on a randomized, multicenter, open-label trial in patients with HER2-positive, operable, locally advanced or inflammatory breast cancer

Brought To You By Singer & Song Writer Kristen Mills (T2-4d). Breast tumor samples were required to show HER2 overexpression (IHC 3+ or FISH amplification ratio of at least 2.0 determined by a central laboratory). The trial enrolled 417 patients who were randomly assigned to receive 1 of 4 neoadjuvant regimens prior to surgery as follows: trastuzumab plus docetaxel; pertuzumab plus trastuzumab and docetaxel; pertuzumab plus trastuzumab; or pertuzumab plus docetaxel.

Pertuzumab, trastuzumab, and docetaxel were administered preoperatively by intravenous infusion (IV) every 3 weeks for a total of 4 cycles. Following surgery all patients received 3 cycles of fluorouracil, epirubicin, and cyclophosphamide (FEC) IV every 3 weeks and trastuzumab was administered IV every 3 weeks to complete 1 year of therapy. The trial’s primary endpoint was pathologic complete response (pCR) rate defined as the absence of invasive cancer in the breast (ypT0/is). The FDA-preferred definition of pCR is the absence of invasive cancer in the breast and lymph nodes (ypT0/is ypN0). PERJETA is a sterile, clear to slightly opalescent, colorless to pale brown liquid for intravenous infusion. Each single use vial contains 420 mg of pertuzumab at a concentration of 30 mg/mL in 20 mM L-histidine acetate (pH 6.0), 120 mM sucrose and 0.02% polysorbate 20.

Some breast cancers have large amounts of a protein called HER2 on the surface of the cells. These cancers are ‘HER2 positive’ and can be treated with a drug called trastuzumab which targets the HER2 protein. You may have trastuzumab with chemotherapy. Paclitaxel anddocetaxel are drugs that doctors often use.

Sam Houston Biotech A Houston Based cancer Research Organization has found that genomic science has advanced. Sections of microarray provide targets for parallel in situ detection of DNA, RNA and protein targets in each specimen on the array. The better News is that Genomics is on the Clock. Genomics provide a faster cheaper more effective way to detect the Her2 gene by using Semiconductor Sequencing. A example of this technique is Gennxeix Biotech Inc Semiconductor Sequencing. "Quantum Theory" In Action for Breast Cancer Patients. One of the major player and touch down makers for breast cancer is Houston Texas Methodist Hospital. In A clinical Trial A Rev. Noel Denison, a retired Methodist minister, was diagnosed with locally advanced HER2-positive breast cancer and is enrolled in the study at Methodist, one of only two locations in the United States. The clinical trial is for locally advanced or metastatic HER2-positive breast cancer and combines standard chemotherapy with trastuzumab emtansine, better known in the breast cancer world as T-DM1, and pertuzumab, a monoclonal antibody that also attaches to HER2 on cancer cells. Using Genomics and semiconductors to detect breast cancer plus T-DM1 to treat breast cancer is a winning combination. What is T-DM1? T-DM1 is in a new class of cancer-fighting agents called antibody drug conjugates. By combining the antibody trastuzumab directly with docetaxel (standard chemotherapy) and/or pertuzumab, the T-DMI is designed to attack the tumor cells directly and deliver the chemotherapy. Trastuzumab emtansine (T-DM1) consists of our proprietary DM1 cancer-killing agent attached to the HER2-binding antibody, trastuzumab, developed by Genentech (a member of the Roche Group) using our linker and methods of attachment. Trastuzumab emtansine is in global development by Roche under a collaboration agreement between ImmunoGen and Genentech. Marketing applications for trastuzumab emtansine are under review in the US and Europe. The Defense and the most dangerous aspect of breast cancer is its ability to spread to distant sites, most tumors are initially unable to do that Learning more specifically what triggers metastases may provide additional targets for preventing and treating the malignant process that causes cancer deaths.

It’s widely accepted that cancers acquire the ability to spread through the gradual accumulation of genetic changes, and experiments have also shown that these changes occur in parallel with changes in the protein content and 3-dimensional patterning of the protein meshwork that creates their immediate surroundings Gene that stops the growth of KCNK9 Genes is gene is p53. p53 is a fundamental determinant of cancer susceptibility, p53 integrates stress signals and elicits apoplectic responses that maintain genomic stability. When cells sense a decrease in oxygen availability (hypoxia), they develop adaptive responses in order to sustain this condition and survive. If hypoxia lasts too long or is too severe, the cells eventually die. Hypoxia is also known to modulate the p53 pathway, in a manner dependent or not of HIF-1 (hypoxia-inducible factor-1), the main transcription factor activated by hypoxia. The p53 protein is a transcription factor, which is rapidly stabilized by cellular stresses and which has a major role in the cell responses to these stresses. This process is why it is important Conrad says for people that are first degree relatives of breast cancer patients, must take a genomic test to see if they are the carrier of gene KCNK9. By identifying this gene we can direct patients with the correct advise as to deal with the fact that they have a lunp on the breast to they are going to get a lump on their breast. Often what happens is that a breast cancer patients dose not go to the doctor or take important test to see if there is a lump on the breast. what happens is the spread of breast cancer is responsible for more than 90 percent of breast cancer deaths.

Pertuzumab is a type of biological therapy called a monoclonal antibody. It works by targeting the HER2 protein but in a different way to trastuzumab. We know from research that having both pertuzumab and trastuzumab together may be better than having just one of them alone.

TDM1 is a combination of trastuzumab and a chemotherapy drug called DM1. Trastuzumab finds the cancer cells and delivers the DM1 to them. This type of drug is called a conjugated monoclonal antibody.

It is clear to Barron’s Medical Journal first year oncologist will have a new way of treating breast cancer all before the end of President Obama second Term

Friday, October 25, 2013

Understanding Natural Hormones in Women

Barron's Medical Journal reporting From Rice University Houston, Texas USA Robert Graham Ph.D. Reporting

Understanding Natural Hormones in Women

Houston, Texas ( AP ) Barron's Medical Journal Interviewed Houston's leading authority on Hormones Dr. Zamora. Dr. Zamora says, the wonderful world of the very special natural hormones a human being can have: Natural Bioidentical Hormones, as multiple research studies have shown.

Natural hormones

Brought To You By Singer & Song Writer Kristen Mills are typically manufactured by biochemists in chemical laboratories. The biochemist extracts the base molecule from plants in their isolated compound forms, and then adds the necessary carbon, oxygen, and hydrogen atoms to the base molecule. The resulting molecule is bio-identical to the human molecule. The hormones produced in this manner are all natural.

The signs of hormonal issues include:

Weight Gain

Fatigue

Memory loss

Miscarriage

Premenstrual syndrome

Infertility

Ovarian cysts

Depression

Insomnia

Water retention

Hair loss

Vaginal dryness

Hot flashes

Low immune system

Reduced libido

Fibroids

Bone and joint conditions

Loss of libido

Let Natural Energy help to bring your body back to homeostasis.

Human hormones are many, but what I call "women hormones" and "men hormones" are not only the best natural chemical a body can have but VERY DIFFERENT to all other chemicals in the body.

If we really care about our brain, our skin, bones, energy, and many brain funcions such as our temperature, memory, and sleep, we need to always have the best hormonal balance in us. It is possible.

The main hormones in women are progesterone and estrogen, and in men is testosterone. It is very important to know that Natural Medicine is a very advanced field nowadays. As a trained physician I always knew about the importance of having normal hormonal levels, but we didn't have natural bioidentical hormones until recently. And as soon as I knew about them, how effective and safe they are, I immediately began helping so many women many years ago.

Bioidentical means these hormones are chemically the same as our human hormones. And very easy to use and to balanced our blood levels. Take advantage! Help your skin, your hair, mood, sleep, energy, bone health and more, much more with Natural Bioidentical Hormones. The results and benefits I know thousand of women and men have got because of them keep me helping many more people.

Brought To You By Dr. Zamora's Hormones The right Hormone level is very important.

Tuesday, October 22, 2013

First Lady Michelle Obama Would Be Proud of University Of South Carolina Falon Tilley Nutrition Research

Barron’s Medical Journal Reporting from Food and Nutrition Conference and Expo at The George R. Brown Convention Center Houston, Texas USA (Global Newswire ) ( PRNewswire )

First Lady Michelle Obama Would Be Proud of University Of South Carolina Falon Tilley Nutrition Research

Houston ( AP ) First Lady Michelle Obama would be Proud of Falon Tilley A Ph.D. Student At the University of South Carolina who research is on display at the Food and Nutrition Conference in Houston, Texas. Ms. Tilley research is focused on After school programs & Summer Camp Lunch Programs. Genomics is now a House Hold name. Genomics is the study of your genes to determine if you have a disease. Barron’s Medical Journal reports on if a patient is diagnosed with breast cancer what are some of the things that friends and family members can do to help the patient through their battle with breast cancer. Nutrition is key says eighty nine percent of the oncologist we spoke with. Now using genomics and minerals like selenium is key to help breast cancer patients.

Women forty years old and who took a genomic test and found that they were going to get breast cancer what are some of the things that you can do As breast cancer realative? Some other concerns that friends and family members can be concerned with is, how many more people must suffer and lose their life to cancer due to ineffective and toxic treatments? Why are research dollars nighty nine percent is directed towards radiation, chemotherapy and other outdated methods? Why is there no room for innovations that use a drug-free and natural approach to healing? Our medical system suffers from excess control from large pharmaceutical corporations, a

Brought To You By Singer & Song Writer Kristen Mills revolving door policy at the FDA and NCI, misdirected and misappropriated funds from cancer foundations and corruption within the American Cancer Society. Cancer is a 200 billion dollar business and there is little incentive to research and develop low-cost treatments based on diet, lifestyle and the use of natural non-patentable compounds. The mission of the Nutritional Oncology Research Institute is to promote a revolutionary approach in clinical oncology

that will lessen needless suffering and enormously lower the cost of cancer treatment. Major steps have already been implemented in developing an effective, low-cost, safe and scientifically sound protocol able to treat a wide range of cancers. With support and funding, these advances will become thenew standard of care in clinical oncology.

Falon Tilley research is interesting if administered as directed breast cancer patients can get breast cancer later rather than sooner. Tilley stress that Afterschool programs (ASPs) are an important setting to increase moderate-to-vigorous activity (MVPA) of children. Policies exist that explicitly target MVPA in the ASP setting. Unfortunately, the majority of children fail to accumulate sufficient amounts of MVPA while attending ASPs. Strategies to increase children's MVPA in ASPs, therefore, are needed. The purpose of this study was to describe the impact of a comprehensive and coordinated approach to improving child MVPA in ASPs.

Four large scale ASPs serving ~500 children participated in a quasi-experimental pre-post study. Observation (System for Observing Play and Leisure Activity in Youth) of child activity levels were collected on 4 nonconsecutive, unannounced days during baseline (Fall 2011) and post-intervention (Spring 2012). The intervention (January-April 2012) consisted of: policy implementation, professional development training, on-site booster sessions and ongoing technical assistance.

MVPA was classified as the “vigorous” SOPLAY category. Random-effects regression models examined the impact of the intervention on the proportion of boys/girls observed in MVPA or sedentary. A total of 4,525 observations were collected. At baseline, 16.1% and 11.4% of boys and girls, respectively, were engaged in MVPA compared to 20.1% and 17.2% at post-intervention. Additionally, at post-intervention, observations demonstrated a decrease of ~10% in sedentary behavior for boys and girls The comprehensive and coordinated approach implemented over 4 months can lead to important changes in the proportion of children in MVPA while also reducing sedentary behavior. Further exposure to the comprehensive approach has the potential to help ASPs meet MVPA goals outlined in polices.

Barron's Medical Journal Interviewed one of Houston Leading Authorities in the Geneis 129 Diet, Jan Jordan a Nutritionist, Jan has taught diet & lifestyle from a biblical prospective for over 12 years & is a Naturopathic Doctor, Certified Nutritionist, Certified Christian Counselor, Raw Food Chef and Halleluhjah Acres Health Minister. She can be contacted at janjordannd@yahoo.com

Jan says we must start with the quote: And God said, Behold, I have given you every herb bearing seed, which is upon the face of all the earth, and every tree, in the which is the fruit of a tree yielding seed; to you it shall be for meat.

Selenium is at the core of this nontoxic cocktail that gently triggers cancer cells to initiate programmed cell death. The specific form of selenium, sodium selenite has been shown in many scientific studies to be able to kill cancer cells while causing no harm to normal healthy cells. This is an enormously important discovery because conventional chemotherapy kills many more normal healthy cells than cancer cells. Two other components of the nutraceutical cocktail act synergistically allowing very low doses of sodium selenite and a very simple schedule of administration.

Two minerals, zinc and selenium, are key in maintaining balance in the body and keeping cancer away. Recent research has added to the pile of data underscoring the importance of these minerals in keeping women cancer-free.

The identification and characterization of functional elements in eukaryotic genomes, primarily using selenium-dependent genes can help breast cancer patients. On the one hand, we develop and apply computational tools to identify selenoproteins and other genomic features. On the other, we use population genetics and molecular evolution approaches to study their evolution. Because nutrition is a prominent selective force in humans and other primates, we are particularly interested in whether differences in dietary selenium have shaped the use and regulation of selenoproteins in these species. We are also interested in more theoretical aspects of sequence evolution

Jan goes on to explain around the year 1999 she went to her primary care Physician and took a Mammogram and was advised to see a Oncologist. Jan decided to take matters in here hands and treat the lump on her breast without consulting a Oncologist. Jan a nutritionist by education started on the Genesis 129 Diet which is just food with seeds and six months later she says that she was cancer free. It is now 14 years later and still cancer free says that this diet works for her and many other folks. The area of concern is that people that start the diet with stage1 or stage 2-breast cancer and go back to eating their normal diet and this is when the breast cancer reoccurs.

Barron’s Medical Journal decided to look in to the science behind the Genesis 129 diet. The association between dietary fat and breast cancer has been examined for a long time; it remains one of the most controversial in nutritional epidemiology (In the early 1940s, animal studies suggested that high-fat diets could stimulate mammary carcinogenesis. This notion was subsequently reinforced by results of international correlation studies and migrant studies; the latter showed that migrant populations that replaced their indigenous low-fat diets with high-fat, Western diets experienced breast cancer incidence rates similar to those of the host populations. Beginning in the mid-1970s, case–control study reports tended to show positive associations between dietary fat intake and breast cancer.

However, the possibility of differential recall of diet between case and control subjects cast doubt on these results Although pooled analyses of subsequent cohort studies failed to show an association between fat intake and the risk of breast cancer a more recent meta-analysis of 14 cohort studies that adjusted for energy intake found that women who consumed the highest levels of total fat had a statistically significant 13% higher risk of breast cancer than those who consumed the lowest levels. Recently reported findings from the Women’s Health Initiative (WHI) Randomized Controlled Dietary Modification Trial provided suggestive evidence that a low-fat diet can reduce the incidence of breast cancer incidence, although follow-up was shorter and the reduction in fat intake in the intervention group, smaller than originally planned. The Geneis diet provided the women with 650 calories (kcal) in the form of two pints of semi-skimmed milk, four portions of vegetables (80g/portion), one portion of fruit, a salty low calorie drink and a multivitamin and mineral supplement. God instructs man to eat (Genesis 1:29). The dense living nutrients found in raw foods and their juices produce abundant energy and vibrant health while satisfying our cells’ nutritional needs, controlling hunger efficiently.

What a great conference so many of the major food companies are spending billions on research that focus on how we eat and what we eat can help with breast cancer.

Tuesday, October 8, 2013

How Susan G. Komen And Personalized Medicine--Genomics Is A Breast Cancer Game Changer

Barron’s Medical Journal Reporting From Boston At Harvard University Beth Israel Medical Center

How Susan G. Komen And Personalized Medicine--Genomics Is A Breast Cancer Game Changer

Boston MA ( AP )Barron’s Medical Journal investigative report on breast cancer fundraising series starts with The Susan G Komen March. With only fifteen percent of the research dollars spent on

Brought To You By Singer & Song Writer Kristen Mills Personalized Medicine, Barron's wants to make all of the new patient’s that is going to get to go the Doctors now that they have Affordable Health Care Act ( Obama Care )

BMJ want to make sure that patients are asking about genomics for breast cancer. DNA methylation patterns can discover three hundred times faster than a mammogram can breast cancer. Breast cancer is one of the most prevalent human malignancies and is a major cause of cancer-related morbidity and mortality. Invasive ductal carcinoma (IDC) of the breast is a phenotypically

diverse disease, consisting of tumors with varying pathologic and molecular characteristics. The primary biological subtypes of IDC include estrogen receptor (ER)– and progesterone receptor (PR)–positive tumors (luminal A and B), tumors that are human epidermal growth factor receptor 2 (HER2)–enriched, and tumors that are ER/PR-negative (basal-like). These molecular determinants have significant effects on metastatic behavior and clinical outcome. For example, ER/PR+tumors are generally associated with better clinical prognosis, whereas basal-like (ER/PR− and HER2−, triple-negative) tumors are associated with higher rates of metastasis and death The genomic alterations, including both genetic and epigenetic aberrations, underlying these differing metastatic potentials are ill-defined.

Significant effort has been undertaken to more accurately define the molecular alterations underlying breast cancer. For example, it has been shown that hormone receptor (HR) status is prognostic for clinical outcome. Mutations in genes such asBRCA1, PTEN, and PIK3CA help promote breast cancer oncogenesis and are enriched in specific subgroups of IDC Genome-wide sequencing surveys have been performed to identify the scope of mutations in breast cancers). These data demonstrate that there exists substantial biological heterogeneity between and within the ER/PR+ and ER/PR− subgroups for which the molecular foundations remain obscure In addition, gene expression classifiers have been developed to help predict metastatic risk). Despite their increasing use in the clinic, the genomic root causes of the transcriptome differences that underlie metastatic potential are unclear.

It is well established that widespread changes in DNA methylation patterns occur during oncogenesis and tumor progression Cancer-specific changes in DNA methylation can alter genetic stability, genomic structure, and gene expression). Promoter CpG island methylation can result in transcriptional silencing and plays an important role in the oncogenic process A CpG island methylator phenotype (CIMP), which is associated with a strong tendency to hypermethylate specific loci, has been described in a subset of colorectal cancers, and recently in a subgroup of gliomas Aberrations in DNA methylation have been reported in human breast cancer, but the impact of the methylome on metastasis and the presence of a B-CIMP have remained elusive To resolve these questions, we conducted a systematic, genome-wide characterization of the breast cancer methylome in breast cancers with diverse metastatic behavior.

Cancer cells undergo massive alterations to their DNA methylation patterns that result in aberrant gene expression and malignant phenotypes. However, the mechanisms that underlie methylome changes are not well understood nor is the genomic distribution of DNA methylation changes well characterized.

Here, we performed methylated DNA immunoprecipitation combined with high-throughput sequencing (MeDIP-seq) to obtain whole-genome DNA methylation profiles for eight human breast cancer cell (BCC) lines and for normal human mammary epithelial cells (HMEC). The MeDIP-seq analysis generated non-biased DNA methylation maps by covering almost the entire genome with sufficient depth and resolution. The most prominent feature of the BCC lines compared to HMEC was a massively reduced methylation level particularly in CpG-poor regions. While hypomethylation did not appear to be associated with particular genomic features, hypermethylation preferentially occurred at CpG-rich gene-related regions independently of the distance from transcription start sites. We also investigated methylome alterations during epithelial-to-mesenchymal transition (EMT) in MCF7 cells. EMT induction was associated with specific alterations to the methylation patterns of gene-related CpG-rich regions, although overall methylation levels were not significantly altered. Moreover, approximately 40% of the epithelial cell-specific methylation patterns in gene-related regions were altered to those typical of mesenchymal cells, suggesting a cell-type specific regulation of DNA methylation. Cancer-specific alterations in DNA methylation are hallmarks of human malignancies; however, the nature of the breast cancer epigenome and its effects on metastatic behavior remain obscure. To address this issue, we used genome-wide analysis to characterize the methylomes of breast cancers with diverse metastatic behavior. Groups of breast tumors were characterized by the presence or absence of coordinate hypermethylation at a large number of genes, demonstrating a breast CpG island methylator phenotype (B-CIMP).

The B-CIMP provided a distinct epigenomic profile and was a strong determinant of metastatic potential. Specifically, the presence of the B-CIMP in tumors was associated with low metastatic risk and survival, and the absence of the B-CIMP was associated with high metastatic risk and death. B-CIMP loci were highly enriched for genes that make up the metastasis transcriptome. Methylation at B-CIMP genes accounted for much of the transcriptomal diversity between breast cancers of varying prognosis, indicating a fundamental epigenomic contribution to metastasis. Comparison of the loci affected by the B-CIMP with those affected by the hypermethylator phenotype in glioma and colon cancer revealed that the CIMP signature was shared by multiple human malignancies. Our data provide a unifying epigenomic framework linking breast cancers with varying outcome and transcriptomic changes underlying metastasis.

Semiconductor Sequencing Chips that create a direct connection between Biochemical and digital information, bringing these two languages together.Hybrid's chips are designed like any other semiconductor chips.

Pairing proprietary semiconductor technology with sequencing chemistry a nucleotide is incorporated into a strand of DNA by a polymerase, a hydrogen ion is released. Hybrid Pharma used a high-density array of micro-machined wells for bioctechnology process in a massive way. Each well holds a different DNA template. Beneath the wells is an ion-sensitive layer and beneath that a proprietary Ion sensor.

When a nucleotide, is added to a DNA template and is then incorporated into a strand of DNA, a hydrogen ion will be released. The charge from that ion will change the pH of the solution, which can be detected. Hybrid's sequencer—essentially will call the base, going directly from Biochemical information to digital information.

If there are two identical bases on the DNA strand, the voltage will be double, and the chip will record two identical bases called.

This process uses no scanners, no cameras, no light—each Nucleotide incorporation is recorded in a real time process.

Panoincell uppressed p53, as it is in many cancers, defective cells multiply, fueling Breast Cancer. p53 can't order a bad cell to kill itself without p63 and p73 also being active.

When metastatic Breast Cancer occurs p63 is inactive.The reactivation of TAp63 could benefit patients with metastatic breast cancer. Make sure you ask your Marcher how much of the money raised at the Susan G. Komen March go to Genomic Science.

Tuesday, October 1, 2013

Breast Cancer Is The Number One Reason Affordable Care Act (ACA) Must Stay In Place Congress

Barron’s Medical Journal Reporting From The Texas State Fair In Dallas Texas USA At The Cotton Bowl The Sight For This Year’s Prairie View A&M University Vs. Grambling State University NCAA Football Game.

Breast Cancer Is The Number One Reason Affordable Care Act (ACA) Must Stay In Place Congress:

Dallas Texas ( AP ) Barron’s Medical Journal is in Dallas asking the question is the team and fans of the Prairie View A&M University Vs Grambling State University Game How many people attending the game will have a relatives that will get breast cancer. Research says it is eighteen percent. Affordable Care Act (ACA) by design is to reduce the rate of eighteen percent in the African American Communities to fewer than five percent of patients that will die one year after diagnoses.

Affordable Care Act (ACA) or Obamacare, is a United States federal statute signed into law by President Barack Obama on March 23, 2010. Together with the Health Care and Education Reconciliation Act

On October 1, 2013 The Health Insurance Marketplace is open! You can now enroll in a health insurance plan that covers essential benefits, pre-existing conditions, and preventive services. Most people who apply for coverage will qualify for lower costs of some kind in the Marketplace. Four things you can do before you apply.

1. Find out how the Marketplace works.

2. Learn how to choose the health insurance plan that’s right for you.

3. Get personal help applying for health coverage.

4. Ask us a question about the Marketplace by phone or live web chat.

Choose a plan that meets your needs and enroll, Coverage starts as soon as January 1, 2014.

Barron’s Medical Journal Ask Rose Conrad Ph.D. C.E.O Of Sam Houston Biotech to talk about how breast cancer works to destroy a patients life. Conrad says that no one dies of breast cancer only when breast cancer spreads to your lungs. If you get a breast cancer genomics test by the age of forty you have a ninety four percent chance to live to sixty. Conrad gose on to say Breast Cancer and HIF-1 Is Why ObamaCare must stay in place. To stop breast cancer from spreading to the patients lungs. Breast cancer spreading to the lungs is the number one reason breast cancer patients expire. Primary Care Physicians and Obama Care is key to prevent women expiring from breast cancer and extend their life.

Sam Houston Biotechnology Scientist Using Genomics has made progress in Houston working with HIF-1. Hypoxia-inducible factor 1 (HIF-1) is a transcriptional activator forbreast cancer. Advances in biochemical purifica- tion, molecular characterization and cellular - molecular biol- ogy ofHIF-1. Sam Houston found involvement in human breast cancer progression, based on the analysis of human breast cancer biopsies and experimental animal mice models. HIF-1 as a therapeutic target can extend the life of many stage four breast Cancer patients.

Sam Houston concern with patients with diabetes and breast cancer may not receive full Benefit of HIF-1. All women having access to a physician can have access to HIF-1. Genomics provide a faster cheaper more effective way to detecting Breast Cancer by using Semiconductor Sequencing. A example of this technique is Sam Houston Semiconductor Sequencing. "Quantum Theory" In Action for Breast Cancer Patients.

A polymerase is an enzyme whose central function is associated with polymers of nucleic acids such as RNA and DNA. The primary function of a polymerase is the polymerization of new DNA or RNA against an existing DNA or RNA template in the processes of replication and transcription. In association with a Sam Houston also uses a Visualize Real-Time Breast Cancer Data using Signal Stochastic Resonance Units Neurons Detection and Analysis for Breast Cancer model after McCulloch-Pitts. Gennxeix. computer-assisted diagnosing of breast cancer from mammograms. Sam Houston works is a genetic network simulation trained with tumor incidence data from knockout experiments.

Sam Houston uses Semiconductor Sequencing Chips that create a direct connection between Biochemical and digital information, bringing these two languages together. Gennxeix's chips are designed like any other semiconductor chips.

Pairing proprietary semiconductor technology with sequencing chemistry a nucleotide is incorporated into a strand of DNA by a polymerase, a hydrogen ion is released. Sam Houston used a high-density array of micro-machined wells for bioctechnology process in a massive way. Each well holds a different DNA template. Beneath the wells is an ion-sensitive layer and beneath that a proprietary Ion sensor.

Genomics can be the GPS to Extend life in Breast Cancer Patients.